Precise Diabetic Wound Therapy: PLS Nanospheres Eliminate Senescent Cells via DPP4 Targeting and PARP1 Activation

Zhao, Renliang; Jin, Xuefeng; Li, Ang; Xu, Bitong; Shen, Yifan; Wang, Wei; Huang, Jinghuan; Zhang, Yadong; Li, Xin

doi:10.1002/advs.202104128

Cited by 24 publications

(12 citation statements)

References 75 publications

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“…The SASP affects cellular interactions in vivo and is inextricably linked to cellular senescence, ageing, and age-related diseases ( Hubackova et al, 2012 ; Zhao et al, 2021 ). The SASP factors can activate the body’s immune system ( Jin et al, 2021 ).…”

Section: Senescence-associated Secretory Phenotype Functional Classif...mentioning

confidence: 99%

The Role of Senescence-Associated Secretory Phenotype in Bone Loss

Zhu

Wan

Yang

et al. 2022

Front. Cell Dev. Biol.

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As the population of most nations have a large proportion of older individuals, there is an increase in the prevalence of osteoporosis. Consequently, scientists have focused their attention on the pathogenic mechanisms of osteoporosis. Owing to an increase in studies on cellular senescence in recent years, research has begun to focus on the function of the senescent microenvironment in osteoporosis. With chronic inflammation, senescent cells in the bone marrow secrete a series of factors known as senescence-associated secretory phenotype (SASP) factors, acting on their own or surrounding healthy cells and consequently exacerbating ageing.The components of the SASP may differ depending on the cause of osteoporosis. This review aimed to summarize the relationship between SASP factors and osteoporosis and suggest new insights into the mechanistic investigation of osteoporosis.

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Section: Senescence-associated Secretory Phenotype Functional Classif...mentioning

confidence: 99%

The Role of Senescence-Associated Secretory Phenotype in Bone Loss

Zhu

Wan

Yang

et al. 2022

Front. Cell Dev. Biol.

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“…2 E). Zhao et al synthesized polyelectrolyte complex nanoparticles for plasmid delivery [ 20 ]. Nanosized SA solids ranged from 0.04% to 0.08%, and higher concentrations resulted in larger agglomerate-like solution systems.…”

Section: Resultsmentioning

confidence: 99%

An IFI6-based hydrogel promotes the healing of radiation-induced skin injury through regulation of the HSF1 activity

et al. 2022

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Radiation-induced skin injury (RISI) is a common complication of radiotherapy. Interferon-alpha inducible protein 6 (IFI6) significantly reduces the radiation sensitivity of HaCaT cells. Sodium alginate (SA) has substantial moisturizing properties. Graphene oxide (GO) is a suitable substrate with physical antibacterial properties. Therefore, we designed materials to modify IFI6 using the biogule of polydopamine (PDA) connected to GO/SA. The structure, size, morphology, and elemental compositions of IFI6-PDA@GO/SA were analyzed. Cytological studies suggested that IFI6-PDA@GO/SA is non-toxic to HaCaT cells, with antibacterial properties. It promotes migration and vascularization and inhibits apoptosis. These cells express IFI6 after irradiation. The mouse model suggested that IFI6-PDA@GO/SA promotes wound healing and reduces reactive oxygen species expression. IFI6-PDA@GO/SA accelerates RISI healing, possibly by initiating the SSBP1/HSF1 signaling pathway. In addition, IFI6-PDA@GO/SA improves the immune microenvironment. This study constitutes the first use of IFI6 as a RISI wound-healing material.

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“…Several potential treatments are already in development to either eliminate senescent cells or minimize their negative effects to accelerate diabetic wound healing. Zhao et al described a nanomaterial that can target senescent cells and induce apoptosis, demonstrating that it could be used to promote diabetic wound healing [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Defective NCOA4-dependent ferroptosis in senescent fibroblasts retards diabetic wound healing

Wei¹,

Liu²,

Zheng³

et al. 2023

Cell Death Discov.

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Cellular senescence describes a state of permanent proliferative arrest in cells. Studies have demonstrated that diabetes promotes the pathological accumulation of senescent cells, which in turn impairs cell movement and proliferation. Historically, senescence has been perceived to be a detrimental consequence of chronic wound healing. However, the underlying mechanism that causes senescent cells to remain in diabetic wounds is yet to be elucidated. Ferroptosis and ferritinophagy observed in diabetes are due to iron metabolism disorders, which are directly associated with the initiation and progression of diabetes. Herein, we reveal that senescent fibroblasts in diabetic wounds are resistant to ferroptosis and that impaired ferritinophagy may be a contributing cause. Further, the expression of NCOA4, a key factor that influences ferritinophagy, is decreased in both diabetic wound tissue and high glucose-induced senescent fibroblasts. Moreover, NCOA4 overexpression could render senescent fibroblasts more vulnerable to ferroptosis. A faster wound healing process was also linked to the induction of ferroptosis. Thus, resistance to ferroptosis impedes the removal of senescent fibroblasts; promoting ferritinophagy could reverse this process, which may have significant implications for the management of diabetic wounds.

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Precise Diabetic Wound Therapy: PLS Nanospheres Eliminate Senescent Cells via DPP4 Targeting and PARP1 Activation

Cited by 24 publications

References 75 publications

The Role of Senescence-Associated Secretory Phenotype in Bone Loss

The Role of Senescence-Associated Secretory Phenotype in Bone Loss

An IFI6-based hydrogel promotes the healing of radiation-induced skin injury through regulation of the HSF1 activity

Defective NCOA4-dependent ferroptosis in senescent fibroblasts retards diabetic wound healing

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